TY  - JOUR
AU  - Bird, MK
AU  - Reid, CA
AU  - Chen, F
AU  - Tan, HO
AU  - Petrou, S
AU  - Lawrence, AJ
Y2  - 2014/05/22
Y1  - 2010/03/01
SN  - 1461-1457
UR  - http://hdl.handle.net/11343/32969
AB  - Drugs of abuse have the ability to instantiate plastic adaptations within the central nervous system, and this property may relate to the development and persistence of addiction. In this context, a single exposure to cocaine in rodents may induce synaptic plasticity by increasing the AMPA/NMDA receptor excitatory post-synaptic current (EPSC) amplitude ratio in dopaminergic cells of the ventral tegmental area (VTA). Here, we examine the role of the metabotropic glutamate 5 (mGlu5) receptor in this regard using a genetic mouse model. The control AMPA/NMDA EPSC ratio is reduced in mGlu5-deficient mice compared to wild-types. Moreover, cocaine-induced enhancement of this EPSC ratio is also absent in mutant mice, which suggests that mGlu5 receptors are required for single-dose cocaine-induced plasticity onto VTA cells. While the temporal profile of hyperactivity to acute cocaine is altered in mGlu5-deficient mice; these mice still develop and express sensitized psychomotor responses to cocaine. These data suggest that the mGlu5 receptor is required for cocaine-induced plasticity in VTA dopaminergic cells. In contrast, the mGlu5 receptor may not be essential for psychostimulant behavioural sensitization; although it probably impacts other aspects drug addiction, such as motivation to self-administer.
LA  - English
PB  - OXFORD UNIV PRESS
KW  - cocaine
KW  - mGlu5 receptor
KW  - sensitization
KW  - synaptic plasticity
KW  - VTA
T1  - Cocaine-mediated synaptic potentiation is absent in VTA neurons from mGlu5-deficient mice
DO  - 10.1017/S1461145709990162
IS  - International Journal of Neuropsychopharmacology
VL  - 13
IS  - 2
SP  - 133-141
L1  - /bitstream/handle/11343/32969/294673_Cocaine-mediated_Lawrence.pdf?sequence=1&isAllowed=y
ER  -